In the later sleep cycles, the MFV changes from one sleep stage to another were less pronounced than in

the first sleep cycle. During the transition from NREM sleep to wakefulness, the MFV remained lower than in the evening pre-sleep stage. Even after the patients awoke the next morning, it took several minutes for the MFV to reach the value measured during the pre-sleep phase of the previous evening. There were no significant side-to-side differences between the left and right MCA. When changes in the sleep stages were provoked using brief tone pulses or clicks, the EEG frequency rose, but the MFV remained low or even decreased for a few seconds before rising to the earlier level. CO2 retention by holding one’s breath or CO2 stimulation will lead

to a vessel dilatation of the cerebral resistance vessels and to a decrease of vascular Talazoparib mouse resistance. Therefore, the relative CO2 reactivity can be defined as the percentage of FV change per percentage of mmHg CO2 change. Although the CO2 test is used as a matter of routine [41] and [42] and although approximately more than 30% of all cerebral ischemias occur at night time, so far little is known about CO2 reactivity during normal sleep. We, therefore, tried to perform a CO2 stimulation during sleep in healthy subjects. During 19 nights the authors [Klingelhöfer J et al., unpublished data] were able to evaluate on 106 CO2 stimulation periods.

In order to be admitted into evaluation, the healthy Roscovitine subjects had to reach at least an end-expiratory CO2 concentration of more than 50 mmHg. They also had to be able to tolerate a CO2 accumulation period for a minimum of 90 s. Fig. 6 shows an original recording of the left MCA of a 23-year-old subject during sleep. The topmost recording demonstrates the original envelope curve, the middlemost the course of MFV and the lowermost the CO2 concentration during CO2 stimulation. The increase of velocity Oxymatrine is clearly visible. From these data the authors calculated the relative CO2 reactivity during different sleep stages for the whole healthy collective. The results show that CO2 stimulation presented no significant differences in light, slow wave and REM sleep as compared to the waking state in healthy subjects. The authors concluded that cerebrovascular CO2 reactivity is maintained during normal sleep. In healthy subjects no significant differences as compared to the waking state have been revealed. During CO2 stimulation in healthy sleepers an increase of mean EEG frequencies in slow wave sleep has been explained as a sign of growing activity within an arousal reaction. A second study examining CO2 reactivity in normal sleep was accomplished by Meadows et al. [43] and [44].